Susceptibility to ovarian endometriosis in Polish population is not associated with HLA-DRB1 alleles

BACKGROUND: Endometriosis is associated with inflammatory autoimmune reactions; however, aetiopathogenesis of the disease is still poorly understood. While autoimmune disorders are often associated with particular HLA alleles, the possible involvement of HLA in the aetiopathogenesis of endometriosis...

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Veröffentlicht in:Human reproduction (Oxford) 2005-04, Vol.20 (4), p.970-973
Hauptverfasser: Roszkowski, Piotr I., Sankowska, Monika, Jałbrzykowska, Agnieszka, Radomski, Dariusz, Drągowska, Katarzyna, Płoski, Rafał, Malejczyk, Jacek
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Sprache:eng
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Zusammenfassung:BACKGROUND: Endometriosis is associated with inflammatory autoimmune reactions; however, aetiopathogenesis of the disease is still poorly understood. While autoimmune disorders are often associated with particular HLA alleles, the possible involvement of HLA in the aetiopathogenesis of endometriosis is still a subject of controversy. The aim of the study was to examine the distribution of HLA-DRB1 alleles in women with endometriosis. To ensure homogeneity of the studied group, only women with ovarian endometrial cysts were included. METHODS: The study included 65 Polish patients of Caucasian origin in whom ovarian endometriosis had been confirmed by laparoscopic and histopathological examinations. HLA-DRB1 alleles were typed using a reverse slot blot method. A frequency of particular HLA-DRB1 alleles in patients was compared with that of a control group of 700 unrelated ethnically matched individuals as well as 193 age-matched women without endometriosis. RESULTS: No statistically significant differences were found in the distribution of HLA-DRB1 alleles in patients with ovarian endometriosis as compared with control populations. CONCLUSIONS: The results of the present study show that ovarian endometriosis is not associated with particular HLA-DRB1 allele(s). This may suggest that aetiology of this form of endometriosis may be not primarily associated with class II HLA-mediated autoimmune reactions.
ISSN:0268-1161
1460-2350
DOI:10.1093/humrep/deh715